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软枣猕猴桃多糖减轻 C57BL/6 小鼠实验性溃疡性结肠炎。

Ficus carica polysaccharide attenuates DSS-induced ulcerative colitis in C57BL/6 mice.

机构信息

Laboratory of Functional Chemistry and Nutrition of Food, College of Food Science and Engineering, Northwest A&F University, Yangling 712100, China.

出版信息

Food Funct. 2020 Jul 1;11(7):6666-6679. doi: 10.1039/d0fo01162b. Epub 2020 Jul 13.

DOI:10.1039/d0fo01162b
PMID:32658237
Abstract

The Ficus carica polysaccharide (FCPS) components of the common fig fruit have been demonstrated to exhibit antioxidant and immunity-enhancing activities. However, it is unclear whether it could prevent the ulcerative colitis development. Here, we reported that 5 week orally administered FCPS (150-300 mg per kg bw) significantly prevented DSS-induced colitis in C57BL/6J mice by improving the colon length and suppressing the infiltration of inflammatory cells in the gut. FCPS treatment protected the goblet cells, elevated the expression of tight junction protein claudin-1, and suppressed the formation of cytokines including TNF-α and IL-1β. FCPS supplementation significantly reformed the gut microbiome by enhancing the abundance of S24-7, Bacteroides, and Coprococus, and suppressing the abundance of Escherichia and Clostridium at the genus level. Consistently, the formation of beneficial microbial metabolites, short chain fatty acids, especially acetate and butyrate, were improved in FCPS-treated colitis mice. The correlation analysis indicated that the protective effects of FCPS on ulcerative colitis might be highly correlated with the microbiota composition changes and the formation of SCFAs. In conclusion, these results indicated that FCPS supplementation could be a promising nutritional strategy for reducing inflammatory bowel disease and the gut microbes play essential roles in providing these beneficial effects.

摘要

无花果多糖(FCPS)是普通无花果果实的成分之一,已被证明具有抗氧化和增强免疫力的活性。然而,目前尚不清楚它是否可以预防溃疡性结肠炎的发生。在这里,我们报道了 5 周口服给予 FCPS(150-300mg/kgbw)可通过改善结肠长度和抑制肠道中炎性细胞的浸润,显著预防 C57BL/6J 小鼠的 DSS 诱导的结肠炎。FCPS 治疗可保护杯状细胞,上调紧密连接蛋白 Claudin-1 的表达,并抑制 TNF-α和 IL-1β等细胞因子的形成。FCPS 补充剂通过增加 S24-7、拟杆菌和粪球菌的丰度,同时抑制大肠杆菌和梭菌属在属水平上的丰度,显著改变了肠道微生物组。一致地,FCPS 处理的结肠炎小鼠中有益微生物代谢产物,特别是乙酸盐和丁酸盐的短链脂肪酸的形成得到改善。相关性分析表明,FCPS 对溃疡性结肠炎的保护作用可能与微生物组成变化和 SCFAs 的形成高度相关。总之,这些结果表明,FCPS 补充剂可能是一种有前途的营养策略,可用于减少炎症性肠病,而肠道微生物在提供这些有益作用方面起着至关重要的作用。

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